Atherosclerosis begins in the wall of the artery with an early abnormality in the lining of the arterial wall called the endothelium. The endothelium helps to maintain the flexibility or elasticity of the artery and normally inhibits the accumulation of lipid and cellular deposits into the arterial wall of the artery.

Arterial Cross-section I:
A normal elastic artery. The walls of arteries (endothelium) are composed of three concentric zones: Tunica adventitia (outer), tunica media (middle), and tunica intima (inner layer). The walls of all arteries (large and small) throughout the body are distensible: they expand and contract as blood pressure waves from the heart pass through the lumen, the passageway for blood within the arterial walls. It is this distensibility that enables the arterial system to act as an elastic reservoir that stores part of the energy of each cardiac contraction, maintaining blood pressure and flow during diastole to perfuse all bodily tissues.

Arterial Cross-section II:
Early stages of atherosclerosis where changes in the arterial wall have begun to impact blood flow and reduce arterial elasticity. The middle zone of the endothelium (tunica media) thickens, and scar tissue forms within. Plaque begins to form causing the tunica intima to become rigid.

Arterial Cross-section III:
Advanced stage of atherosclerosis. Arterial elasticity is reduced and plaque formation has restricted blood flow within the artery. Plaque invades the tunica media. Plaque can now cause minimal strokes (transient ischemic attacks) due to diminished blood flow (ischemia) to parts of the brain; angina from partly obstructed coronary arteries; or pain in the leg muscles when walking, a result of poor blood supply to the legs (peripheral arterial disease). Blood clots, which tend to occur at the sites of atherosclerotic narrowing, can totally block a vessel and cause a stroke or heart attack.

Abnormal function of the endothelium and the associated structural changes in the wall result in a loss of elasticity of the small arteries. Detection of this loss in elasticity can identify individuals with abnormal arterial structure and function long before plaque formation can cause morbid cardiovascular events. Furthermore, demonstration of normal arterial structure and function might suggest that the individual does not have early atherosclerosis and may not need aggressive risk factor management.

Risk factors
A number of risk factors for atherosclerosis have been identified, including elevated blood pressure, elevated cholesterol level, smoking, diabetes and a family history of atherosclerosis. Clinical events associated with atherosclerosis, including heart attacks (myocardial infarction), strokes, angina (myocardial ischemia), peripheral vascular ischemia (claudication) and renal failure are late manifestations of the disease as a result of plaque formation that impinges on blood flow.

Some specific risk factors:

  • A family history of CV disease/death

  • A family history of CV disease/morbid obesity

  • A family history of diabetes

  • Smoking

  • A family history of elevated cholesterol

  • A sedentary lifestyle

  • A family history of "high" blood pressure

The absence of a clinically applicable method to detect the presence of atherosclerosis prior to plaque obstruction of the lumen (the inner space in the blood vessel through which blood passes) has led to widespread efforts to identify the risk factors in the entire population and to intervene on those who harbor such risk factors.

It is a well-known clinical finding that elastic and flexible arteries are healthy vessels, and that stiff and hardened arteries are not healthy.